FUBP1 antibody - middle region (ARP35704_P050) | Application: IHC, WB | FUBP1 is strongly supported by BioGPS gene expression data to be expressed in Human HepG2 cells | Alias: FBP; FUBP
Complete information for FUBP1 gene (Protein Coding), Far Upstream Element Binding Protein 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
FUBP1 antibody - center region (OAAB10426) | Application: WB | Tested with: Jurkat | Alias: FUBP1; Far upstream element-binding protein 1; DNA helicase V
Complete information for KHSRP gene (Protein Coding), KH-Type Splicing Regulatory Protein, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Rabbit Polyclonal Anti-FUBP1 Antibody. Nucleus without Nucleoli Marker. Validated: WB, ChIP, ICC/IF, IHC, IHC-P, IP. Tested Reactivity: Human, Mouse. 100% Guaranteed.
Mao Q, Stinnett HK, Ho RK. Asymmetric cell convergence-driven zebrafish fin bud initiation and pre-pattern requires Tbx5a control of a mesenchymal Fgf signal. Development. 2015 Dec 15; 142(24):4329-39 ...
J:92194 Li Y, Zhang H, Choi SC, Litingtung Y, Chiang C, Sonic hedgehog signaling regulates Gli3 processing, mesenchymal proliferation, and differentiation during mouse lung organogenesis. Dev Biol. 2004 Jun 1;270(1):214-31 ...
J:173650 Sgantzis N, Yiakouvaki A, Remboutsika E, Kontoyiannis DL, HuR controls lung branching morphogenesis and mesenchymal FGF networks. Dev Biol. 2011 Jun 15;354(2):267-79 ...
Signalment: 5-year-old, female, brown-eared pheasant (Crossoptilon mantchuricum). History: This animal was from a zoo, and was found dead. Its general body condition was poor.. Gross Pathology: The cecal wall was diffusely thickened and nodular.. Contributors Diagnosis and Comments: Cecum: Typhlitis, granulomatous, with mesenchymal proliferation around Heterakis isolonche.. Histology: The submucosa is widely expanded by the presence of well-circumscribed, discrete, irregularly-sized, and highly cellular nodules which impinge on the mucosa and tunica muscularis. Most of them are composed of small interlacing bundles of elongated fibroblast-like cells around one or a few sections of a nematode parasite. Onion-like arrangements around blood vessels are sometimes observed. The cells show an open-faced nucleus, a prominent nucleolus and an eosinophilic, sometimes vacuolated, cytoplasm.. The nematode is typical of Heterakis isolonche: polymyarian coelomyarian musculature, triradiate intestine, ...
Oligodendrogliomas are the second most common malignant brain tumor in adults and exhibit characteristic losses of chromosomes 1p and 19q. To identify the molecular genetic basis for this alteration, we performed exomic sequencing of seven tumors. Among other changes, we found that the CIC gene (homolog of the Drosophila gene capicua) on chromosome 19q was somatically mutated in six cases and that the FUBP1 gene [encoding far-upstream element (FUSE) binding protein] on chromosome 1p was somatically mutated in two tumors. Examination of 27 additional oligodendrogliomas revealed 12 and 3 more tumors with mutations of CIC and FUBP1, respectively, 58% of which were predicted to result in truncations of the encoded proteins. These results suggest a critical role for these genes in the biology and pathology of oligodendrocytes ...
More mutations in the two genes were found in an additional 27 oligodendroglioma samples. In all, two-thirds of the samples studied had CIC and FUBP1 mutations.. "Whenever we find genes mutated in a majority of tumors, it is likely that the pathway regulated by that gene is critical for the development and biology of the tumor," Nickolas Papadopoulos, Ph.D., associate professor of oncology at the Johns Hopkins Kimmel Cancer Center, was quoted as saying.. In brain cancer, the Hopkins investigators say CIC and FUBP1 mutations may be the "missing link" in what scientists describe as a "two-hit" theory of cancer development. The theory is based on the fact that each cell in the human body has two copies of 23 chromosomes containing thousands of protein-producing genes. If a gene on one chromosome is damaged or deleted, the other copy makes up for the loss of protein. But if the second copy fails as well, the cell cannot make the proper protein and may become cancerous.. In oligodendrogliomas, the ...
The Ja-panese TeX Devel-op-ment Com-mu-nity sub-mit-ted an up-date to the js-classes pack-age. Ver-sion num-ber: 2017-10-04 Li-cense type: bsd Sum-mary de-scrip-tion: Classes tai-lored for use with Ja-panese An-nounce-ment text ...
Relevance of male-to-female sex mismatch in liver transplantation for primary biliary cirrhosis. - Michał Grąt, Zbigniew Lewandowski, Waldemar Patkowski, Karolina Maria Wronka, Karolina Grąt, Maciej Krasnodębski, Joanna Ligocka, Hanna Zborowska, Marek Krawczyk
Sex determinations are diverse in vertebrates. Although many sex-determining genes and pathways are conserved, the mechanistic roles of these genes and pathways in the genetic sex determination are not well understood. DAX1 (encoded by the NR0B1 gene) is a vertebrate specific orphan nuclear receptor that regulates gonadal development and sexual determination. In human, duplication of the NR0B1 gene leads to male-to-female sex reversal. In mice, Nr0b1 shows both pro-testis and anti-testis functions. We generated inheritable nr0b1 mutation in the zebrafish and found the nr0b1 mutation caused homozygous mutants to develop as fertile males due to female-to-male sex reversal. The nr0b1 mutation did not increase Caspase-3 labeling nor tp53 expression in the developing gonads. Introduction of a tp53 mutation into the nr0b1 mutant did not rescue the sex-reversal phenotype. Further examination revealed reduction in cell proliferation and abnormal somatic cell differentiation in the nr0b1 mutant gonads at ...
Disorders of sex development (DSDs) are congenital conditions resulting in atypical chromosomal, gonadal or anatomic sex. Around 80% of 46,XY DSD cases still remain unexplained genetically. Phenotypes include gonadal dysgenesis, male-to-female sex reversal and hypospadias, where the urethra is abnormally positioned along the penis. Mutations in SOX9, a gene essential for testicular development, have been implicated in DSDs, but its tissue-specific regulation is not fully understood. SOX9 tissue-specific enhancer mutations can cause isolated clinical phenotypes. Through genome wide mapping, mutations around SOX9 have been identified in isolated DSD patients. All patients had gonadal defects and hypospadias. We hypothesised that a 78 kb region encompassing these mutations contains a novel gonadal enhancer that we aimed to identify. Comparative genomic analysis identified seven highly conserved sub-regions within TES2. Unexpectedly, transgenic mouse analysis revealed that the most highly conserved ...
Wilhelm D., Martinson F., Bradford S., Wilson M.J., Combes A.N., Beverdam A., Bowles J., Mizusaki H., Koopman P.. We have raised an antibody specifically recognizing endogenous mouse SRY protein and used it to investigate the molecular and cellular mode of action of SRY in testis determination. We find that expression of SRY protein closely mirrors the expression of Sry mRNA in mouse genital ridges and is detectable for 6 to 8 h after the mRNA ceases to be detectable. The subset of somatic cells that expresses SRY begins to express SOX9 almost immediately. Since these SOX9-positive cells go on to develop as Sertoli cells, it appears that SRY expression marks the pre-Sertoli cell lineage and leads to up-regulation of Sox9 expression cell-autonomously. However, a small proportion of SOX9-positive cells did not appear to express SRY, possibly reflecting the additional involvement of paracrine signaling in activating Sox9 transcription in these cells. We confirmed by ex vivo cell mixing experiments ...